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This project, based on a established youth-led volunteering model is expanding as a result of self-referrals and is being delivered in Hackney, Haringey and Tower Hamlets. It will support young people aged 13 to 25 to deliver volunteering and social action projects which they have identified to be of benefit to the local community. The aim of project is that all of the young people who are participating in it will develop key skills and have positive experiences that will shape their personal development.

Certain bacterial species can colonise to form biofilms- large structures which protect bacteria from physical and chemical removal e.g. antibiotics. If adhered to biomedical implants, bacteria can cause repeated infections which couldn't be treated by antibiotics and therefore would lead to the removal of the implant. In some patients, this would result in repeated invasive surgery. Our interest is in crystalline biofilms which can block urinary catheters and cause catheter-associated urinary-tract-infections (CAUTI). The main bacterium causing CAUTI is E. Coli in which E. Niba et al. (2008) isolated 110 genes involved in the formation of biofilms. Mutations in key genes will be created using Lambda red recombination which is a highly efficient and well established method for creating precise gene deletions. Deletions will be confirmed using PCR and sequencing. The deletion mutants will be analysed for biofilm formation using a bioflux system which generates shear force by continuous flow of liquid. This is an open system ensuring nutrients are available and thereby favouring biofilm formation. Both pathotypes and their respective mutants will be tested for the capacity to form biofilms at a range of temperatures. Data from the above experiments will be quantified using ImageJ software.

Metastasis is the major driver of mortality in cancer patients. A common feature that potentiates the dissemination of cancer cells is the enhanced secretion of tumorigenic effector proteins. Malignant secretion can be mediated by the phosphoinositides (PIs) family of lipids in conjunction with PI regulator proteins that bind to or act upon each PI. One such PI regulator is phosphatidylinositol transfer protein cytoplasmic 1 (PITPNC1). PITPNC1 is highly upregulated in many human cancers and involved in the promotion of metastasis. The PITPNC1-dependent recruitment of RAB1B, a GTPase, to the Golgi-compartment is known to enhance secretory capacity and drives the release of pro-metastatic proteins. The goal of the project is to validate the reported interaction between PITPNC1 and RAB1B in vitro. To this end, recombinant PITPNC1 and RAB1B will be expressed in Vmax™ Express cells and purified by affinity and size exclusion chromatographies. This will allow validation of the reported interaction by pull-down. Additional insights will be gained from assessing the PITPNC1-RAB1B interaction in solution by performing a NMR chemical shift perturbation experiment using 15N-labelled RAB1B. The effects of lipid/nucleotide exchange on the interaction will also be explored. These studies may contribute to the development of therapies specific to metastatic disease.

I will address three questions crucial to tackling child health inequalities (HIs): What factors lie on the causal pathway between socio-economic circumstances and children’s health and parental health-related behaviours, and which are most likely to reduce HIs? Who: Can we better predict those most likely to develop poor health (and will this help to target interventions more fairly and efficiently)? How: To what extent can early years’ interventions, if rolled out at different scales (e.g. to everyone, those living in deprived areas, those at greatest risk), reduce HIs? Cutting-edge methods, and the novel application of traditional methods, will be applied in two complementary data sources: linked administrative data (in Greater Glasgow and Clyde – the UK’s largest health governing board and subject to the highest HIs in Western Europe) and three UK cohorts (Millennium Cohort Study, Growing Up in Scotland, Southampton Women’s Survey). Several aspects of child health (motor, social, cognitive and motor development; thinness, overweight and obesity; unintentional injuries) and parental health-related behaviours (immunisation; breastfeeding; smoking) will be examined. Maternal mental health, childcare and parenting will be investigated as mediating mechanisms that are amenable to intervention through early years’ services. Findings will inform local and national policy and practice.

Tendinopathies pose a significant, prevalent and costly musculoskeletal medicine challenge. Tendinopathy is dominated by a switch from Collagen type I to type III production resulting in biomechanically inferior tendon ultrastructure. My previous studies, invoking several model systems, directly implicate inflammatory cytokines, dysregulated apoptosis and biomechanical cellular stress in pathology. MicroRNAs (miRNAs) are short non-coding RNA that post-transcriptionally regulate gene expres sion. They are increasingly recognised to manifest central roles in a variety of human pathologies but have never been investigated in tendinopathy. MiR29 family members have however been implicated as regulators of collagen III synthesis. I recently detected significantly altered levels of miR29 family members, correlated with collagen matrix dysregulation and inflammatory infiltrate in damaged human tendon. I hypothesise that modulation of miR29 represents a novel therapeutic approach to tendon healing. I aim: 1. To define the role of miR 29 in experimental and clinical tendinopathy 2. To identify cellular pathways regulated by mir-29a in tenocytes, and by which mechanism. 3. To develop and validate targeted therapy for miR-29a using sponge technology as a miR delivery system in experimental tendon injury. Thus, I will clearly elucidate the role of miRNA 29 in tendinopathy and in so doing, define its therapeutic utility.

The concept of 'attentiveness' - the emptying of one's self for attunement with the other, and, more broadly, a habit of mental openess and awareness - has rich implications in healthcare, creative writing, and literary, historical, and philosophical scholarship within the related fields of the Medical Humanities and Literature and Medicine . This conference adopts the term attentive writers as evocative of the multitude of both professional and non-professional caregivers - clinical and no n-clinical healthcare workers - whose attention to illness might take narrative form. By bringing the established field of inquiry on the physician as writer into dialogue with current calls for a more inclusive approach to the Medical Humanities, the conference aims to question the authoritative place of the Western - traditionally male - physician in our explorations of the health/humanities interface. The relationship between healthcare, authorship and authority will be addressed through three strands of enquiry: (1) an historical and literary examination of 'attentive writers'; (2) a more devolved interrogation of the field of Narrative Medicine; and (3) an examination of 'attentive writing' as creative practice. This international conference at Glasgow University, aims to stimulate and bring together research and practice (clinical and creative) on this exciting topic.

The University of Glasgow and NHS Greater Glasgow & Clyde together provide an outstanding environment for basic and clinical research with a strong focus on translation. This will be greatly enhanced by the opening of the new 900M South Glasgow Hospital, which will be one of Europe's largest hospitals. We will develop a modern, multidisciplinary CRF, co-located with critical care and imaging facilities, focusing on experimental medicine, phase I and II clinical trials and biomarker development . The CRF will allow us to combine our strengths in inflammation, cardiovascular medicine, oncology, neurology and child health to develop a world leading centre in proof of concept studies into chronic degenerative diseases, stratified medicine, biomarker discovery and target validation. Our ability to link core datasets and outcomes will underpin these approaches, as will the early inclusion of our biostatisticians and health economists in the design, planning and execution of clinical trial s. The juxtaposition of world class researchers with a population of high morbidity will allow us to fully exploit the exciting opportunities of the new South Glasgow Hospital to deliver benefit to patients locally, nationally and internationally. The CRF will also offer a rich training environment for clinical research fellows and clinical lecturers.

Objectives: This cataloguing and preservation project will open up the research possibilities of the papers of Victor Douglas Eustace Webb (1915-c2004), who was involved in the Scottish allotment scene for over 50 years, and was instrumental in the setting up of Scottish Allotments Scheme for the Unemployed (SASU). In particular it will support research in relationto the recently awarded 'Ground-breaking: Community Heritage in Glasgow's allotments' PhD Studentship under the Arts and Humanities Research Council's Collaborative Doctoral Award (CDA) Scheme http://www.gla.ac.uk/schools/humanities/latestnews/headline_278338_en.html Details of work: The Project Archivist will catalogue the collection to item-level to fully unlock the research potential. To promote the collection's long-term preservation, it will be repackaged in acid-free folders and boxes. Ferrous clips and staples will be replaced with brass paperclips.

I am requesting a small grant to conduct archival research relating to a project on the cultural history of cocaine and the public image of medical practitioners in the late nineteenth and early twentieth centuries. This project will examine how cocaine functioned symbolically as a representation of both the most admirable, and the most alarming personal attributes of the modern medical professional. I will examine rare materials held at Edinburgh University Library, the British Library, and the Wellcome Library in London. My research centres on two significant historical personages and their connection to the opposing facets of cocaine discourse: Sir Robert Christison, whose pathological researches were one inspiration for the character of Sherlock Holmes; and Dr Thomas Neill Cream, serial poisoner, and potential Jack the Ripper suspect. In examining heretofore unpublished papers including Christison's own observations on the stimulant effects of coca, I elucidate important links b etween these two men, their experiences with cocaine, and the transforming image of the Victorian medical man. I will also conduct research into the surgical applications of cocaine and the manner in which these impacted the popular conception of the new, technologically-innovative chemical compound.

Globally, 170 million people are infected with hepatitis C virus (HCV). A vaccine and new treatment strategies for are therefore highly desirable. Much work on the mechanisms underlying spontaneous control of HCV (15-50% of those infected) has been carried out, but this has been based on small patient groups (typically 10-20 individuals) as early HCV infection rarely presents clinically. Small human and animal studies have highlighted the role of the T-cell response in spontaneous clearance. I now have the opportunity to investigate the determinants of spontaneous clearance and progression to chronicity in a large well-characterised cohort of patients with acute HCV infection. The key research goals of this project are to identify conserved and variable regions of the HCV genome during early infection, to characterise the phenotype, specificity and function of T-cells during evolving spontaneous clearance and to correlate changes within the viral quasispecies with adaptive immune res ponses over time. I will use deep sequencing to amplify the whole HCV genome and will link changes in viral population structure with T cell responses using flow cytometry, ELISpot analysis and the HCV replicon system.

How are protein thiol groups modified in the endoplasmic reticulum during protein folding and cell stress? The folding and assembly of proteins within the endoplasmic reticulum (ER) is an essential process for normal healthy tissues. Breakdown in this process leads to several chronic diseases so it is critical that we have a better understanding of the molecular details of how cells fold proteins that enter the secretory pathway. Nearly a third of all proteins coded for by the human genome enter the secretory pathway and undergo disulfide formation during their folding. We know that members of the protein disulfide isomerase family catalyse disulfide formation but we know little about the function of each of the family members or how the unique redox environment of the ER is maintained. In addition, a variety of modifications to thiol groups can regulate protein function yet we know very little about the targets of these modifications in the ER or their consequence on protein fu nction. This proposal aims to dissect the molecular mechanisms involved in this process by investigating key questions concerning disulfide formation and thiol modification that remain unanswered. Specifically these include: How are the redox conditions in the endoplasmic reticulum balanced to allow correct folding and assembly of proteins entering the secretory pathway? What is the specific role of protein disulfide isomerase family members during protein folding and degradation? What are the targets for reversible thiol modification in the ER? What are the sources and levels of thiol-modifying chemicals? Which enzymes catalyse the reversal of thiol modification? The results from this work will impact on our understanding of how the cellular protein folding machinery functions and will clarify the role of thiol modification of proteins within the ER.

Control of endemic and emerging pathogens is hampered by inadequate understanding of pathogen diversity and the mechanisms driving transmission within and between species. Molecular sequence data are increasingly available and promise to revolutionize this uncertainty, but analytical tools to integrate evolutionary data into mechanistic models of disease dynamics are needed. I have established a research programme in Peru that tracks rabies virus exposure histories in vampire bats through spatia lly replicated, longitudinal surveys, together with detailed case reports and sequence data from hundreds of rabies outbreaks in livestock. In this fellowship, I will expand and integrate these data to link the spatio-temporal dynamics of viral persistence within bats to patterns of cross-species emergence. I will partner with the Peruvian government to estimate of the burden and risk factors of livestock rabies, allowing economic valuation and informed distribution of limited resources, while e mpowering national surveillance data to parameterize mechanistic models linking viral persistence and emergence. These models will be applied to explore the efficacy of potential oral vaccination and culling campaigns for rabies control. A final goal will establish a framework to explore patterns of viral transmission and evolution between ecologically linked species (bats, livestock) by conducting genomic surveillance of sentinel animals.

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